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Cerebral Palsy

Hyperbaric Medicine Officially Enters the Prohibition Era

 

Hyperbaric Medicine Officially Enters the Prohibition Era

An article specifically written for ”Hyperbaric Medicine Today”
in their “Physicians’ Forum Counterpoint” feature.
From Volume 1 Issue 1
Research in Hyperbaric Medicine by Dr. Eric P. Kindwall

Dr. Paul G Harch writes:

The Physicians' Forum article in the inaugural issue is a comprehensive discourse with many good points on the legality of off-label HBOT, research funding, a registry, recommendations for patients seeking off-label treatment, and standardized testing/documentation. However, these points are nearly lost in an extremely confusing, obfuscating tangle of terms definitions, and concepts that is partly based on a double standard. Despite the confusion, the message and threat to the entire hyperbaric medicine community was transmitted so loud and clear in the final paragraph that I was moved to declare this the “Prohibition Era Of Hyperbaric Medicine” It appears that the purpose of the article is to alter the historical method of the practice of medicine and hyperbaric medicine by jeopardizing a physician's membership in a medical society should they dare to use HBOT for an off-label indication.

The article begins with a comment on “evidence-based medicine”' and then proceeds to speak about peer-reviewed, randomized, prospective, controlled, double-blinded trials (RCPT's) to assess validity of scientific information. The double standard in these two paragraphs can be appreciated in the 1996 approval of intracerebral abscess (ICA), (cerebral abscess, subdural empyema, and epidural empyema) by the Hyperbaric Oxygen Therapy Committee to the accepted indications list. The argument in the 1996 HBOT Committee Report was based on thirteen cases treated off-label, ten of which were published in the Journal of Hyperbaric Medicine, 1989. These were combined with six cases generated after years of open solicitation from an influential HBOT Committee member to any UHMS physician who had treated cerebral abscess with hyperbaric oxygen. These last six cases are strongly biased since very few physicians are willing to volunteer a personal/professional failure, i.e., a hyperbaric oxygen treated cerebral abscess case that died. The mortality from these twenty cases was compared to the latest figures, 1991, on the historical declining mortality rate in cerebral abscess to achieve statistical significance and approve cerebral abscess as an accepted indication. To summarize, the accepted indication, cerebral abscess, is a diagnosis composed of three separate diseases, based on twenty non controlled cases, none of which appear to be on an JRB-approved protocol, all of which were apparently treated off-label, only ten of which are in a peer reviewed journal, six of which are highly biased, non-published solicitations and the argument for which is based on a comparison to a historical declining mortality rate. Regardless of the strong pathophysiological argument this is weak science, especially when compared to data discussed below. To subsequently argue, in the Physicians' Forum article's lead paragraph for evidence-based medicine from randomized prospective controlled research published in peer-reviewed journals as an intro and backdrop to a critique of HBOT/cerebral palsy and off-label use of HBOT, is a double-standard.The article disparages the Hyperbaric Oxygen treatment data of cerebral palsy children by labeling it “anecdotal”

The double standard is more apparent in the article's review of HBOT cerebral palsy data. The article disparages the hyperbaric oxygen treatment data of cerebral palsy children by labeling it "anecdotal." This "anecdotal" experience includes six reports: 240 "anecdotal" cases by Machado, a single "anecdotal" case reported by me in 1994 (the first cerebral palsy case treated with HBOT in North America), three "anecdotal" cases reported by Dr. Neubauer and me at a hyperbaric meeting in Buenos Aires in 1996, an additional "anecdotal" case reported by Neubauer and me in the Third Edition of K.K. Jain 's Textbook of Hyperbaric Medicine in July/99, 18 "anecdotal" predominantly IRB cases reported by me at the Boca Raton July 1999 Conference, and now 25 IRB "anecdotal" cases reported by Montgomery at McGill in 1999. While a number of the above reports are abstracts, three of the studies (Machado, Harch, and Montgomery) are prospective and controlled (each patient serving as his own control). The Montgomery study also used blinded examiners and was published in a peer reviewed journal. This constitutes greater experience for HBOT treatment of cerebral palsy than for the nineteen "anecdotal" HBOT/ICA cases which generated inclusion on the accepted indications list in 1996. To disparage the evidence for HBOT/CP is inconsistent.

Harch HBOT for Infant Problems with the Brain or Brain Trauma: Shaken Baby Syndrome, Cerebral Palsy CP, Infant Brain Injury

HBOT for an Infant/Child Brain Injury

According to Dr. Harch, "HBOT for infants is no different than HBOT for adults except that infants can be exquisitely sensitive to oxygen and thus, require careful dosing." In the early 1990s Dr. Harch began an investigation of hyperbaric oxygen therapy in pediatric brain injury.  Beginning with the first cerebral palsy (CP) child he applied HBOT and SPECT brain blood flow imaging (discussed below) to any child with a neurological diagnosis primarily involving the brain. What he found was that HBOT acted like a generic drug on a multitude of different brain disorders in children, including genetic disorders.

Harch HBOT in Cerebral Palsy and Pediatric Neurology: A Scientific Perspective

This article will review the current literature and history of application of low pressure (low dosage) LPHBOT to pediatric neurology. The most rigorous study on this subject will be analyzed and its interpretation debated in terms of past and present scientific data and theoretical considerations. The major flaw in the study's conclusion is illustrated by pre and post HBOT SPECT brain imaging on two of the author's cerebral palsy patients and the author's 12-year-experiehce of HBOT treatment of Cerebral Palsy children. There is substantial scientific explanation and data to argue for reimbursement of HBOT in Cerebral Palsy.

Hyperbaric Oxygen Therapy in the Management of Cerebral Palsy

HBOT in the Management of Cerebral Palsy

Virginia Neubauer, Richard Neubauer and Paul Harch

 

An entry from K.K. Jain's Textbook Of Hyperbaric Medicine

Cerebral palsy is a chronic neurological disorder that can be due to several causes of brain damage in utero, in the perinatal period, or postnatally. Hyperbaric oxygen has been shown to be useful in treating children with cerebral palsy. This topic is discussed under following headings:
Causes of Cerebral Palsy
Oxygen Therapy in the Neonatal Period
Treatment of Cerebral Palsy with HBOT
Conclusions

 

Causes of Cerebral Palsy
 

The term cerebral palsy (CP) covers a group of non-progressive, but often changing, motor impairment syndromes secondary to lesions or anomalies of the brain arising in the early stages of development. Between 20 to 25 of every 10,000 live-born children in the Western world have the condition (Stanley et al 2000). Problems may occur in utero, perinatal, and postnatal. Infections, traumatic brain injury, near-drowning and strokes in children suffering from neurological problems come under the heading of cerebral palsy. Diagnosis of cerebral palsy resulting from in utero or early perinatal causes may be made immediately after birth, but more commonly occurs between 15 and 24 months. It is possible that CP may be misdiagnosed for years because specific symptoms may show up very late in childhood. Some of the possible causes of Cerebral Palsy and are listed in Table 21.1.
Although several antepartum causes have been described for CP, the role of intrapartum asphyxia in neonatal encephalopathy and seizures in term infants is not clear. There is no evidence that brain damage occurs before birth. A study using brain MRI or post-mortem examination was conducted in 351 full-term infants with neonatal encephalopathy, early seizures, or both to distinguish between lesions acquired antenatally and those that developed in the intrapartum and early postpartum period (Cowan et al 2003). Infants with major congenital malformations or obvious chromosomal disorders were excluded. Brain images showed evidence of an acute insult without established injury or atrophy in (80%) of infants with neonatal encephalopathy and evidence of perinatal asphyxia. Although the results cannot exclude the possibility that antenatal or genetic factors might predispose some infants to perinatal brain injury, the data strongly suggest that events in the immediate perinatal period are most important in neonatal brain injury. These findings are important from management point of view as HBOT therapy in the perinatal period may be of value in preventing the evolution of cerebral palsy.

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